Changes in the production of IL-10 and TNF-alpha in skeletal muscle of rats with heart failure secondary to acute myocardial infarction.


Journal Article

BACKGROUND: Recent studies show that the expression of inflammatory mediators, such as cytokines, is an important factor for the development and progression of heart failure (HF), especially in the presence of left ventricular dysfunction. These changes have been demonstrated both in the plasma and heart muscle and, more recently, in skeletal muscle of rats and in patients with HF. OBJECTIVE: To investigate the production and expression of tumor necrosis factor-alpha (TNF) and interleukin-10 (IL-10) in the soleus and the extensor digitorum longus (EDL) muscles of animals with left ventricular dysfunction after myocardial infarction (MI). METHODS: We used male Wistar rats that underwent ligation of the left coronary artery without reperfusion. Four weeks after this procedure, the animals underwent echocardiography and were divided into the following experimental groups: sham operated (sham) and IM. They remained under observation for a further period of 8 weeks. RESULTS: The level of the cytokine TNF-alpha increased by 26.5% (p <0.05), and its gene expression increased 3 times (p <0.01). The level of IL-10 decreased by 38.2% (p <0.05). Both changes occurred only in the soleus muscle, with no change in the EDL. The decrease (36.5%, p <0.05) in the IL-10/TNF-alpha ratio was due to both increased tissue levels of TNF-alpha and decreased tissue levels of IL-10. CONCLUSION: Our results showed significant changes in the IL-10/TNF-alpha ratio, which may have an additive role in the assessment of deterioration and progression of left ventricular dysfunction post-MI. Furthermore, our study suggests that these changes seem to be related to the muscle fiber type.

Full Text

Duke Authors

Cited Authors

  • Lopes, RD; Batista, ML; Rosa, JC; Lira, FSD; Martins, E; Shimura, AY; Brum, PC; Lancha, AH; Seelaender, MCL; Lopes, AC

Published Date

  • March 2010

Published In

Volume / Issue

  • 94 / 3

Start / End Page

  • 293 - 320

PubMed ID

  • 20730256

Pubmed Central ID

  • 20730256

Electronic International Standard Serial Number (EISSN)

  • 1678-4170

Digital Object Identifier (DOI)

  • 10.1590/s0066-782x2010000300006


  • eng por

Conference Location

  • Brazil